Microbial desalination cell with sulfonated sodium (poly(ether ether ketone) as cation exchange membranes for enhancing power generation and salt reduction

© 2018 Microbial desalination cell (MDC) is a bioelectrochemical system capable of oxidizing organics, generating electricity, while reducing the salinity content of brine streams. As it is designed, anion and cation exchange membranes play an important role on the selective removal of ions from the desalination chamber. In this work, sulfonated sodium (Na+) poly(ether ether ketone) (SPEEK) cation exchange membranes (CEM) were tested in combination with quaternary ammonium chloride poly(2,6-dimethyl 1,4-phenylene oxide) (QAPPO) anion exchange membrane (AEM). Non-patterned and patterned (varying topographical features) CEMs were investigated and assessed in this work. The results were contrasted against a commercially available CEM. This work used real seawater from the Pacific Ocean in the desalination chamber. The results displayed a high desalination rate and power generation for all the membranes, with a maximum of 78.6 ± 2.0% in salinity reduction and 235 ± 7 mW m−2 in power generation for the MDCs with the SPEEK CEM. Desalination rate and power generation achieved are higher with synthesized SPEEK membranes when compared with an available commercial CEM. An optimized combination of these types of membranes substantially improves the performances of MDC, making the system more suitable for real applications

Investigation of patterned and non-patterned poly(2,6-dimethyl 1,4-phenylene) oxide based anion exchange membranes for enhanced desalination and power generation in a microbial desalination cell

© 2017 The Authors Quaternary ammonium poly(2,6-dimethyl 1,4-phenylene oxide) (QAPPO) anion exchange membranes (AEMs) with topographically patterned surfaces were assessed in a microbial desalination cell (MDC) system. The MDC results with these QAPPO AEMs were benchmarked against a commercially available AEM. The MDC with the non-patterned QAPPO AEM (Q1) displayed the best desalination rate (a reduction of salinity by 53 ± 2.7%) and power generation (189 ± 5 mW m− 2) when compared against the commercially available AEM and the patterned AEMs. The enhanced performance with the Q1 AEM was attributed to its higher ionic conductivity and smaller thickness leading to a reduced area specific resistance. It is important to note that Real Pacific Ocean seawater and activated sludge were used into the desalination chamber and anode chamber respectively for the MDC – which mimicked realistic conditions. Although the non-patterned QAPPO AEM displayed better performance over the patterned QAPPO AEMs, it was observed that the anodic overpotential was smaller when the MDCs featured QAPPO AEMs with larger lateral feature sizes. The results from this study have important implications for the continuous improvements necessary for developing cheaper and better performing membranes in order to optimize the MDC

Longitudinal analysis of blood DNA methylation identifies mechanisms of response to tumor necrosis factor inhibitor therapy in rheumatoid arthritis

Epigenetics; Rheumatoid arthritis; Treatment responseEpigenètica; Artritis reumatoide; Resposta al tractamentEpigenética; Artritis reumatoide; Respuesta al tratamientoBackground Rheumatoid arthritis (RA) is a chronic, immune-mediated inflammatory disease of the joints that has been associated with variation in the peripheral blood methylome. In this study, we aim to identify epigenetic variation that is associated with the response to tumor necrosis factor inhibitor (TNFi) therapy. Methods Peripheral blood genome-wide DNA methylation profiles were analyzed in a discovery cohort of 62 RA patients at baseline and at week 12 of TNFi therapy. DNA methylation of individual CpG sites and enrichment of biological pathways were evaluated for their association with drug response. Using a novel cell deconvolution approach, altered DNA methylation associated with TNFi response was also tested in the six main immune cell types in blood. Validation of the results was performed in an independent longitudinal cohort of 60 RA patients. Findings Treatment with TNFi was associated with significant longitudinal peripheral blood methylation changes in biological pathways related to RA (FDR<0.05). 139 biological functions were modified by therapy, with methylation levels changing systematically towards a signature similar to that of healthy controls. Differences in the methylation profile of T cell activation and differentiation, GTPase-mediated signaling, and actin filament organization pathways were associated with the clinical response to therapy. Cell type deconvolution analysis identified CpG sites in CD4+T, NK, neutrophils and monocytes that were significantly associated with the response to TNFi. Interpretation Our results show that treatment with TNFi restores homeostatic blood methylation in RA. The clinical response to TNFi is associated to methylation variation in specific biological pathways, and it involves cells from both the innate and adaptive immune systems.This study was funded by the Instituto de Salud Carlos III

Interactions between rheumatoid arthritis antibodies are associated with the response to anti-tumor necrosis factor therapy

Terapia anti TNF; Autoanticuerpos; Artritis reumatoideTeràpia anti TNF; Autoanticossos; Artritis reumatoideAnti-TNF therapy; Autoantibodies; Rheumatoid arthritisBackground Blocking of the Tumor Necrosis Factor (TNF) activity is a successful therapeutic approach for 50–60% of rheumatoid arthritis (RA) patients. However, there are yet no biomarkers to stratify patients for anti-TNF therapy. Rheumatoid factor (RF) and anti-cyclic-citrullinated antibodies (anti-CCP) have been evaluated as biomarkers of response but the results have shown limited consistency. Anti-carbamylated protein (anti-CarP) and anti-peptidylarginine deiminase type 4 (anti-PAD4) antibodies have been much less studied. Despite being linked to common immune processes, the interaction between these markers has not been evaluated yet. Our aim was to analyze the interaction between these four antibodies in relation to the response to anti-TNF therapy. Methods For this objective, a prospective cohort of n = 80 RA patients starting anti-TNF therapy was recruited. Serum determinations at baseline were performed for RF, anti-CCP, anti-CarP and anti-PAD4 antibodies using enzyme-linked immunosorbent assays (ELISA). The clinical response to anti-TNF therapy was determined at week 12 using the change in DAS28 score. Association was performed using multivariate linear regression adjusting for baseline DAS28, sex and age. Results The interaction between pairs of antibodies was tested by the addition of an interaction term. We found two highly significant antibody interactions associated with treatment response: anti-CarP with anti-PAD4 (p = 0.0062), and anti-CCP with RF (p = 0.00068). The latter antibody interaction was replicated in an independent retrospective cohort of RA patients (n = 199, p = 0.04). Conclusions The results of this study suggest that antibody interaction effects are important factors in the response to anti-TNF therapy in RA.This project was supported by UCB Pharma

Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)

In 2008, we published the first set of guidelines for standardizing research in autophagy. Since then, this topic has received increasing attention, and many scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Thus, it is important to formulate on a regular basis updated guidelines for monitoring autophagy in different organisms. Despite numerous reviews, there continues to be confusion regarding acceptable methods to evaluate autophagy, especially in multicellular eukaryotes. Here, we present a set of guidelines for investigators to select and interpret methods to examine autophagy and related processes, and for reviewers to provide realistic and reasonable critiques of reports that are focused on these processes. These guidelines are not meant to be a dogmatic set of rules, because the appropriateness of any assay largely depends on the question being asked and the system being used. Moreover, no individual assay is perfect for every situation, calling for the use of multiple techniques to properly monitor autophagy in each experimental setting. Finally, several core components of the autophagy machinery have been implicated in distinct autophagic processes (canonical and noncanonical autophagy), implying that genetic approaches to block autophagy should rely on targeting two or more autophagy-related genes that ideally participate in distinct steps of the pathway. Along similar lines, because multiple proteins involved in autophagy also regulate other cellular pathways including apoptosis, not all of them can be used as a specific marker for bona fide autophagic responses. Here, we critically discuss current methods of assessing autophagy and the information they can, or cannot, provide. Our ultimate goal is to encourage intellectual and technical innovation in the field